Elsevier

New Ideas in Psychology

Volume 41, April 2016, Pages 18-22
New Ideas in Psychology

Systemizing in autism: The case for an emotional mechanism

https://doi.org/10.1016/j.newideapsych.2016.01.001Get rights and content

Highlights

  • Increased systemizing — attempts to build and understand rule-based systems — appears to be a hallmark of autism.

  • Unusually intense emotions, positive and negative, are behind the increased systemizing, says the present hypothesis.

  • A parsimonious mechanism is described, leading from hyper-emotionality to increased systemizing.

  • Several predictions arise from the hypothesis, some already supported by the extant literature.

Abstract

More often than others, people with autism engage in systemizing – attempts to understand and build rule-based systems. The mechanism behind the increased frequency of such behavior in autism is unknown, however. The assumption has long existed that emotions exist to motivate behavior, and there is now much evidence that people with autism tend to have stronger, more easily elicited emotions than the average person. This appears to be the cause of increased systemizing in autism – through a negative and a positive emotional pathway: There is evidence that autistic people want control more strongly than do others. This is often so, says the hypothesis, because strong negative emotions, other things equal, make lack of control feel more aversive than it does for most people. Systemizing can increase the feeling of control and hence reduce the negative emotion. Positive emotion can also motivate systemizing in autism – fascination and attraction more strongly felt and more easily elicited than in other people.

Introduction

Some seventy years ago, Asperger (1944) claimed that autism is an extreme variant of the male intelligence and character. This remained a hypothesis based on a limited number of clinical observations until Baron-Cohen, 2002, Baron-Cohen et al., 2011) launched his extreme male brain theory, arguing that autism can be understood as an exaggerated variant of the male brain. Not all psychological sex differences will be exaggerated in autism, says the theory, but there will be less of everything having to do with empathy, and more of all that has to do with systemizing (Baron-Cohen et al., 2011).

Systems can be numerical, mechanical, natural, social, or belong to several other categories – and systemizing, says Baron-Cohen (2012), is the drive to understand or build systems, which are by definition rule-based. A machine is a system, so is mathematics – and dance, too, can be a rule-based system.

The drive to systemize is assumed to explain central aspects of autistic behavior (Baron-Cohen, 2003, Baron-Cohen, 2010). Though still controversial, Baron-Cohen's theory has generated a considerable amount of research, which in general appears supportive (Baron-Cohen et al., 2011, Nettle, 2007, Wei et al., 2013), though not without exception (Pellicano et al., 2011).

There are several possible causes behind the increased tendency to systemize: Androgens are known to affect brain structure and function (Genazzani, Pluchino, Freschi, Ninni, & Luisi, 2007), and positive correlations have been found between autistic behavior and the level of.

testosterone as well as other sex steroids (Baron-Cohen, 2010, Baron-Cohen et al., 2015). There are also other hypotheses, not necessarily incompatible with the androgen theory, that may help explain why aspects of the autistic brain and behavior appear hypermasculinized – an interesting example being the possible role of gene variants on the X chromosome (Nava et al., 2012).

A central question is still unanswered, however. If we assume that the drive called systemizing is indeed unusually strong in people with autism, how can that be? It is well and good that causative processes may have to do with an unusually masculinized brain – but systemizing is described as a drive, and a “drive,” says an uncontroversial definition, is an “internal source of motivation that impels an organism to pursue a goal or to satisfy a need” (Colman, 2014). What is lacking is an account of why structures and functions thought to characterize an autistic brain give rise to the specific drive to systemize, and what the nature of this drive might be. The present hypothesis attempts to remedy this by describing an emotional mechanism that brings us nearer to several missing answers in a parsimonious fashion.

Section snippets

Presentation of the hypothesis

Most people prefer order (or system) to chaos – and much human progress has been based on the construction of social, legal, and political systems. We are often curious, and may wonder how systems such as locomotives or organisms work. We want to know and control – and as do other organisms, we like most things to be predictable, so we go far to reduce uncertainty (Anselme, 2010). Still people differ, and some are more strongly motivated than others by the chance to understand, construct, and

Testing the hypothesis

The increased tendency to systemize in people with autism is caused by unusually strong and easily elicited feelings, says the present hypothesis. The logical way of testing this claim is to experimentally manipulate the tendency to respond with strong emotion and measure the effect on systemizing.

Though autism could well result from different etiologies, much evidence now indicates that central features of this condition may be caused by an increased ratio of excitatory to inhibitory synaptic

Implications

Above, we saw Baron-Cohen's (2003) proposition that people with autism systemize in order to achieve increased control. This is probably correct, but it is not clear if people with autism want control more than others, and if they do, why this is so.

If the present hypothesis is true, it gives provisional answers to the questions above: Autistic people do want control more than others. They do so because strong negative emotions, other things equal, makes lack of control (or potential lack of

Acknowledgment

Thanks are due to Francisco Pons for helpful comments on an earlier version of the manuscript.

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